Document Detail


Exercise-induced cardiac performance in autoimmune (type 1) diabetes is associated with a decrease in myocardial diacylglycerol.
MedLine Citation:
PMID:  22797313     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
One of the fundamental biochemical defects underlying the complications of diabetic cardiovascular system is elevation of diacylglycerol (DAG) and its effects on protein kinase C (PKC) signaling. It has been noted that exercise training attenuates poor cardiac performance in Type 1 diabetes. However, the role of PKC signaling in exercise-induced alleviation of cardiac abnormalities in diabetes is not clear. We investigated the possibility that exercise training modulates PKC-βII signaling to elicit its beneficial effects on the diabetic heart. bio-breeding diabetic resistant rats, a model reminiscent of Type 1 diabetes in humans, were randomly assigned to four groups: 1) nonexercised nondiabetic (NN); 2) nonexercised diabetic (ND); 3) exercised nondiabetic; and 4) exercised diabetic. Treadmill training was initiated upon the onset of diabetes. At the end of 8 wk, left ventricular (LV) hemodynamic assessment revealed compromised function in ND compared with the NN group. LV myocardial histology revealed increased collagen deposition in ND compared with the NN group, while electron microscopy showed a reduction in the viable mitochondrial fraction. Although the PKC-βII levels and activity were unchanged in the diabetic heart, the DAG levels were increased. With exercise training, the deterioration of LV structure and function in diabetes was attenuated. Notably, improved cardiac performance in training was associated with a decrease in myocardial DAG levels in diabetes. Exercise-induced benefits on cardiac performance in diabetes may be mediated by prevention of an increase in myocardial DAG levels.
Authors:
Rajprasad Loganathan; Lesya Novikova; Igor G Boulatnikov; Irina V Smirnova
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-07-12
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  113     ISSN:  1522-1601     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2012 Sep 
Date Detail:
Created Date:  2012-09-03     Completed Date:  2013-07-08     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  817-26     Citation Subset:  IM    
Affiliation:
Department of Physical Therapy and Rehabilitation Science, University of Kansas Medical Center, Kansas City, Kansas 66160-7601, USA.
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MeSH Terms
Descriptor/Qualifier:
Amino Acid Sequence
Animals
Diabetes Mellitus, Type 1 / metabolism*
Diglycerides / antagonists & inhibitors*,  biosynthesis,  metabolism*
Male
Molecular Sequence Data
Myocardium / metabolism*
Physical Conditioning, Animal / methods,  physiology*
Protein Kinase C / physiology
Random Allocation
Rats
Ventricular Function, Left / physiology*
Grant Support
ID/Acronym/Agency:
HD02528/HD/NICHD NIH HHS; P20 RR016475/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/1,2-diacylglycerol; 0/Diglycerides; EC 2.7.1.-/protein kinase C beta; EC 2.7.11.13/Protein Kinase C
Comments/Corrections

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